This article will address: Diagnosis of metabolic alkalosis and assessment of compensation. Approach to differential diagnosis/ underlying cause of metabolic alkalosis. Metabolic Alkalosis Diagnosis Elevated pH (>7.42) Elevated serum HCO3- (>26) Elevated pCO2 (compensation) What you will initially see (either in the hospital or outpatient setting) is an elevated serum HCO3. This can
Nutrition is an important part of managing chronic dialysis patients so much so that each unit has a registered dietician. Things that I focus on when rounding on a dialysis patient include: Albumin - Malnutrition and protein energy wasting Potassium Bicarbonate - Acid Base status Vitamins - B complex/ C Diabetes Albumin -
MPGN is not a specific disease, it is a pattern of injury seen on light microscopy of kidney biopsy. Membrano - Diffuse thickening of glomerular capillary walls Proliferative - Increased number of cells in the glomeruli Therefore MPGN is when glomeruli have both thickened capillary walls and an increased number of cells. This
You’ve evaluated an acid base disorder. You diagnosed a metabolic acidosis: pH: Low Serum Bicarbonate (HCO3): Low pC02: Low How do you figure out what caused it? This article will provide a framework for differential diagnosis - looking at the: Anion Gap - Is it elevated? Delta - Delta - What’s that? Osmolar
Anemia is an almost universal finding in patients with End Stage Renal Disease requiring dialysis. The following factors contribute: Erythropoietin deficiency: The kidneys normally secrete erythropoietin which stimulates the bone marrow to produce red blood cells. When the kidneys fail, erythropoietin deficiency occurs with resultant anemia. Iron deficiency: Patients on hemodialysis have ongoing
IgA Nephropathy may be the most common glomerulonephritis (GN) in the world. It is most common in East Asians (Chinese and Japanese), relatively common in Caucasians and relatively rare in people of African descent. IgA nephropathy can have a wide range of presentations with variable prognosis. This article will discuss: Clinical presentations Prognosis
Nephrotoxicity from Chemotherapy There are many different mechanisms of nephrotoxicity from chemotherapeutic drugs. These include indirect and direct renal toxicity. Indirect mechanisms Prerenal AKI due to hypovolemia from chemo induced nausea, vomiting, and diarrhea Ischemic acute tubular necrosis (ATN) from neutropenic sepsis or cytokine release syndrome (seen in CAR-T therapy) Direct mechanisms Nephrotoxic
Arteriovenous access is the preferred access for hemodialysis (as opposed to use of a catheter). There are 2 types of arteriovenous access Arteriovenous fistula (AVF) - native artery transposed to native vein. Native vein hypertrophies under increased arterial pressure. This becomes fistula. This is the preferred dialysis access (over both catheters and arteriovenous
Membranous nephropathy is an important cause of nephrotic syndrome in adults. This condition is exciting in nephrology because the pathogenic antibody for the majority of cases of primary idiopathic membranous nephropathy has been discovered. This is the phospholipase A2 receptor (PLA2R) antibody. Clinical Presentation Often presents as full blown nephrotic syndrome with severe
Two parts of trusting your gut: If something doesn’t make sense it probably isn’t right. Take a step back and look again. Don’t go along with something you don’t believe. What is the FeNa? The FeNa is the percent of sodium filtered by the kidneys (glomeruli) that is excreted in the urine. What
